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缩醛磷脂可抑制神经炎症并促进认知功能。

Plasmalogens inhibit neuroinflammation and promote cognitive function.

作者信息

Hossain Md Shamim, Mawatari Shiro, Fujino Takehiko

机构信息

Institute of Rheological Functions of Food, 2241-1 Kubara, Hisayama-machi, Kasuya-gun, Fukuoka 811-2501, Japan.

Institute of Rheological Functions of Food, 2241-1 Kubara, Hisayama-machi, Kasuya-gun, Fukuoka 811-2501, Japan.

出版信息

Brain Res Bull. 2023 Jan;192:56-61. doi: 10.1016/j.brainresbull.2022.11.005. Epub 2022 Nov 5.

DOI:10.1016/j.brainresbull.2022.11.005
PMID:36347405
Abstract

Neuroinflammation (NF) is defined as the activation of brain glial cells that are found in neurodegenerative diseases including Alzheimer's disease (AD). It has been known that an increase in NF could reduce the memory process in the brain but the key factors, associated with NF, behind the dysregulation of memory remained elusive. We previously reported that the NF and aging processes reduced the special phospholipids, plasmalogens (Pls), in the murine brain by a mechanism dependent on the activation of transcription factors, NF-kB and c-MYC. A similar mechanism has also been found in postmortem human brain tissues with AD pathologies and in the AD model mice. Recent evidence showed that these phospholipids enhanced memory and reduced neuro-inflammation in the murine brain. Pls can stimulate the cellular signaling molecules, ERK and Akt, by activating the membrane-bound G protein-coupled receptors (GPCRs). Therefore, recent findings suggest that plasmalogens could be one of the key phospholipids in the brain to enhance memory and inhibit NF.

摘要

神经炎症(NF)被定义为在包括阿尔茨海默病(AD)在内的神经退行性疾病中发现的脑胶质细胞的激活。已知NF的增加会降低大脑中的记忆过程,但与NF相关的、导致记忆失调的关键因素仍然难以捉摸。我们之前报道过,NF和衰老过程通过一种依赖于转录因子NF-κB和c-MYC激活的机制,减少了小鼠大脑中特殊的磷脂——缩醛磷脂(Pls)。在患有AD病理的人类死后脑组织和AD模型小鼠中也发现了类似的机制。最近的证据表明,这些磷脂可增强小鼠大脑的记忆力并减轻神经炎症。Pls可通过激活膜结合的G蛋白偶联受体(GPCRs)来刺激细胞信号分子ERK和Akt。因此,最近的研究结果表明,缩醛磷脂可能是大脑中增强记忆力和抑制NF的关键磷脂之一。

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